|Number Seven, May 2002 - MONTHLY FEATURES|
Physiologic Derangements in Anabolic Steroid Abuse Part 2|
Mark W. Rodacker, MD PhD and Lawrence Maile, PhD
(copyright Maile/Rodacker, 2002)
As discussed in part one, the use of anabolic steroid abuse began in large scale with Russian strength athletes in the 1950s (Voy, R and Deeter, KD 1991) and since has not fallen off despite efforts at education of and by the medical community, legislation, and out of meet drug testing to name a few. In fact, according to several studies outlined in the American Academy of Pediatrics Policy Statement (Johnson, SJ et al. 1997), at best it may have slowed it's pace of increase or leveled off (Figure 1. from National Institute of Drug Abuse). Despite the fact that knowledgeable people in the medical community have been acknowledging that anabolic androgenic steroids (AAS) work to increase muscle mass and strength, while warning of their side effects now for many years (see the policy statements of the American Academy of Pediatrics 1989, and the American College of Sports Medicine 1977 and 1984), the message seems to have fallen on deaf ears in the general public. Perhaps this should have occurred much sooner to prevent a credibility gap from developing between the public's perception of AAS relative safety and the message sent by the medical community. In any event, we see AAS use in the powerlifting community all too frequently and we have personally and collectively seen many of the serious side effects they can produce. Thus we have set forth herein part two to outline the harmful side effects of AAS abuse so that anyone entering into their abuse is well informed by credible information and not that passed out by "gurus" or other abuser's hearsay.
2. Increased strength
3. Decreased recovery time
4. Increased aggression
5. Promote healing of injuries
6. Maintain the same "advantage" as one's opponent
7. Obtaining a winning edge
Cholestasis (bile obstruction)
Peliosis hepatis (Bloody liver cysts)
Oligospermia/azospermia (Few/no sperm)
Gynecomastia (breast enlargement)
Teratogenicity (harm to fetus)
Increased rate of muscle strains and tendon rupture
Striae (stretch marks)
Hirsutism (body and facial hair growth)
Male pattern baldness
Edema (water retention)
Subcutaneous abscess (from non-sterile injection)
Deepening of the voice (female)
Decreased HDL cholesterol ("good cholesterol")
Increased blood pressure
Interstitial fibrosis (scar-like tissue in heart muscle)
Psychologic (see previous article this series)
Aggressiveness ("roid rage")
Hepatitis B or C; HIV infection (if needles are shared)
Decreased immunosurveillance (immune system detection of tumors)
Figure 3a Systemic effects of AAS abuse
Figure 3b Systemic effects of AAS abuse
Figure 4 Polypharmacy in AAS abuse
AAS appear to make the heart wall (muscle) thicker (hypertrophic) with training just as it makes the skeletal muscles enlarge. Within certain parameters this is not necessarily detrimental. The hearts of naturally trained athletes are also enlarged quite commonly. However, in the AAS abuser, several events often take place. Hyperlipidemia and increased total cholesterol, due to much increased LDL (so called "bad cholesterol") is seen as well as decreased HDL (so called "good cholesterol"). This leads to accelerated atherosclerosis such that coronary artery blockage occurs putting the abuser at increased risk of coronary artery thombosis (clotting) and myocardial infarction (hear attack). Moreover, the thickened myocardium tends to accumulate interstitial fibrosis (collagen fiber deposition between the muscle cells much like a scar)( Karch, SB 1997). This is also seen in stimulant abuse and if AAS and stimulants are used in conjunction (as they frequently are), the problem is exacerbated. This can lead to dangerous cardiac conduction problems (irregular heart rhythm) and increased blood flow demands. However, because of coronary artery atherosclerosis (narrowed heart arterial supply of blood) blood flow demands may not be compensated which leads to increased risk of heart attack. Also, sex steroids (AAS and "the pill") occasionally lead to intracardiac thrombosis (clots within the pumping chambers) which can prove fatal suddenly or lead to cerebral infarcts (strokes). This may be seen especially in those who have predisposing genetic conditions which favor clot formation, which actually are not that uncommon in the general public. In addition, AAS cause an increase in the volume of red blood cells and make platelets stickier both of which predispose to a hypercoagulable state in the circulation, i.e., increased risk of clotting. Furthermore, high blood pressure is commonly seen in AAS abusers which further increases the heart wall thickness slowly over time so that effective blood flow to end organs (heart, brain, liver, kidney) can be maintained much like increasing the horsepower needed to pump the same volume of fluid through a smaller hose. This of course, only puts the AAS abuser at an even greater increased risk of heart disease. Numerous case reports exist in the literature describing the deaths of young AAS abusers due to cardiac causes as well as for those who have been long term abusers. This is perhaps the most serious area that AAS abusers will be harmed, often with no realization until very late, if at all.
Figure 5 Myocardial infarct (see black arrow)
Figure 6 Atherosclerosis and thrombosis of coronary arteries
Figure 7 Atherosclerosis of coronary arteries
Because the liver is the primary organ of metabolism for AAS it is not surprising that it can suffer from the toxic effects of abuse, the worst of which are seen with oral (17- alkylated compounds) due to the "first pass" effect, see article one. Finding mildly Elevated liver enzymes are of questionable significance if it is an isolated finding as highly trained athletes can also see some mild elevations, especially if the sample is drawn in proximity to exercise. This is roughly analogous to elevated creatinine levels in muscular individuals. However, monitoring the degree of elevation, the pattern of enzymes involved and levels over time can be helpful. A strong association of peliosis hepatis with AAS does exist. In this condition blood filled cysts make the liver (and sometimes other organs such as the spleen, lung, lymph nodes, and bone marrow sponge-like). Usually this is asymptomatic and may go away after discontinuance of AAS but occasionally people have bled to death. AAS (and the "pill") have been known to induce hepatic adenomas (benign tumors composed of liver cells). This is not a particularly uncommon finding. However, because they also are typically asymptomatic, unless they bleed or are strategically placed anatomically to be felt or compress vital structures, they seldom come to clinical attention. Hepatic coma and carcinoma are rare but have been noted in association with AAS use. If AAS abusers share needles the risk of becoming infected by hepatitis B and C as well as HIV is a very real danger. Cholestasis (bile accumulation) leading to jaundice can be seen with AAS abuse, especially with 17-alkylated compounds. The fact that most AAS (in the USA) are underground produced rather than pharmaceutical grade (up to 1% impurity allowed) or even veterinary grade (up to 5% impurity allowed), leaves one only to imagine what abusers could be exposing themselves to (Musshoff, F Daldrup, T and Ritsch, M, 1997).
Figure 8 Hepatic adenoma
This area is poorly understood but it appears that AAS abuse predisposes to a general decrease in immune function. This is somewhat paradoxical in that AAS are anabolic. As such one would think they would boost the immune system rather than inhibit it as do catabolic steroids such as corticosteroids. Nonetheless, this effect is unpredictable and perhaps depends on the particular AAS used, etc. Tumor cells are occasionally produced in all of us in various tissues but our immune system is always looking to destroy them so that they never develop into dangerous growths. In the AAS abuser we occasionally see this function slip somewhat (increased hepatomas, etc.). In addition, some tumors seem to be fueled by androgens and the abuser thus accelerates their growth and development, e.g., prostatic carcinoma.
The skin and its other structures (adnexae) are androgen sensitive as is the breast which is actually just a modified sweat gland. Thus the major effects seen with AAS abuse are acne (caused by bacterial infection of the skin pores due to excess oil production), gynecomastia in males (nonreversable) and breast atrophy in females. Striae (stretch marks), are also seen as with corticosteroids. These are seen in increased muscle mass in non- AAS users as well so it appears to be an exaggerated effect rather than a specific one. Alopecia (thinning hair) is also seen in males and females in a male pattern of hair loss in sensitive individuals. That is, those with androgen sensitive hair follicles will see premature and accelerated hair loss on the scalp. Bloating or edema is common in AAS abusers giving a significant pinkish "puffy" look. Finally, hirsutism (increased body hair growth) is also seen and is especially evident in females and is usually nonreversible.
Figure 9 Acne and Male pattern hair loss
Figure 10 Gynecomastia
The psychologic effects of AAS abuse can be profound in some individuals and is discussed in depth in other articles in this series. Likewise, the reproductive effects have been previously discussed in part one. Although this discussion is not exhaustively complete we have addressed the most serious and the most common issues related to the pathologic effects of AAS abuse.
Better education, more effective testing such as universal OMT (out of meet testing), increased research, improved collective social conscience, and consistent penalization both legally and through sports sanctioning bodies will form the cornerstones of future AAS abuse determent. To this end the USAPL has been and will remain devoted.